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社交挫败应激与大鼠腰椎间盘突出模型中痛觉行为的关系。

Involvement between social defeat stress and pain-related behavior in a rat lumbar disk herniation model.

机构信息

Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Fukushima, Japan.

出版信息

Eur Spine J. 2020 Oct;29(10):2431-2440. doi: 10.1007/s00586-020-06533-1. Epub 2020 Jul 22.

DOI:10.1007/s00586-020-06533-1
PMID:32700124
Abstract

INTRODUCTION

Psychological and social factors are involved in the disability and chronicity of pain. Our study aim was to investigate whether social defeat stress (SDS) as a psychophysical stress affected mechanical withdrawal thresholds in the lumbar disk herniation (LDH) rat model. Changes in microglia and astrocytes, which play important roles in neuropathic pain states, were also investigated.

MATERIALS AND METHODS

For the LDH model, nucleus pulposus (NP) was applied to the L5 dorsal root ganglion (DRG) in adult female Sprague-Dawley rats. SDS was performed 15 min daily for 8 days. Mechanical withdrawal thresholds were measured, and immunoreactive cells of glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule-1 (Iba-1), which were used as markers of microglia, satellite glial cells, and astrocytes, were assessed in the DRG, spinal cord (SC), and ventrolateral periaqueductal gray matter (VLPAG).

RESULTS

Mechanical withdrawal thresholds decreased in the NP group for 21 days and for 35 days in the NP + SDS group. Expression of GFAP and Iba-1 in the DRG and SC increased up to day 21 in the NP and NP + SDS groups. In the sham + SDS and NP + SDS groups, expression of GFAP in the VLPAG decreased until day 35.

CONCLUSION

SDS prolongs mechanical allodynia induced by NP. Changes of GFAP expression in the VLPAG were associated with mechanical allodynia of the NP + SDS group during the late phase. These results suggest that psychological chronic stress might delay recovery from mechanical allodynia induced by the LDH model.

摘要

简介

心理和社会因素与疼痛的残疾和慢性有关。我们的研究目的是调查作为一种心理生理应激的社会挫败应激(SDS)是否会影响腰椎间盘突出症(LDH)大鼠模型中的机械性退缩阈值。还研究了在神经病理性疼痛状态中起重要作用的小胶质细胞和星形胶质细胞的变化。

材料和方法

对于 LDH 模型,将髓核(NP)施加于成年雌性 Sprague-Dawley 大鼠的 L5 背根神经节(DRG)。每天进行 15 分钟的 SDS,共 8 天。测量机械退缩阈值,并评估 DRG、脊髓(SC)和腹外侧导水管周围灰质(VLPAG)中胶质纤维酸性蛋白(GFAP)和离子钙结合衔接分子-1(Iba-1)的免疫反应性细胞,这些细胞作为小胶质细胞、卫星胶质细胞和星形胶质细胞的标志物。

结果

NP 组的机械退缩阈值在 21 天和 NP+SDS 组的 35 天下降。NP 和 NP+SDS 组的 DRG 和 SC 中 GFAP 和 Iba-1 的表达在第 21 天增加。在假手术+SDS 和 NP+SDS 组中,VLPAG 中的 GFAP 表达在第 35 天减少。

结论

SDS 延长 NP 引起的机械性痛觉过敏。VLPAG 中 GFAP 表达的变化与 NP+SDS 组在后期的机械性痛觉过敏有关。这些结果表明,心理慢性应激可能会延迟 LDH 模型引起的机械性痛觉过敏的恢复。

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